Myocardiogenesis will be studied in normal and cardiac non-function mutant Mexican salamanders (Ambystoma mexicanum) and in normal and cardiomyopathic Syrian Golden Hamsters (strain B10 14.6). The primary objectives of the studies are to learn more about the sequence of events and mechanism(s) of myofibrillogenesis and to determine how inductive interactions operate to control normal heart differentiation. Immuno-electron microscopy using peroxidase-labelled antibodies will provide a means for detecting the sites of formation and subsequent relocation of the different muscle proteins in developing heart cells. Radio-immunoassay will be used to quantify absolute amounts of the proteins; this could establish the stoichiometric relationship required among the contractile and modulatory proteins for normal myofibril formation and muscle function. Tissue culture will be employed in combination with the above methods to study the nature of inductors and repressors of cardiac development. The use of these two unique genetic abnormalities will hopefully provide the "tools" necessary for determining what is required for normal myofibrillogenesis and for the initiation of myoblast function to occur. The special problems associated with the mutations may provide a key for understanding how inductors act on genes to control myoblast differentiation. In a broader sense, these vertebrate "birth defects" are potentially capable of providing an answer to one of the major unsolved problems of modern biology; the control of gene expression in animals. BIBLIOGRAPHIC REFERENCES: Lemanski, L.F. 1977. Morphological and biochemical abnormalities in hearts of cardiac mutant salamanders (Ambystoma mexicanum). J. Supramolecular Structure. In press. Lemanski, L.F., B.S. Marx, and C.S. Hill. 1977. Anterior endoderm morphology in embryonic cardiac mutant salamanders (Ambystoma mexicanum): Evidence for abnormal heart induction. Science. In press.